KIAA1429-mediated ZFPM2-AS1 mA modification promotes the proliferation, migration and invasion of osteosarcoma cells.

Osteosarcoma is the most prevalent malignant bone tumor in pediatric and adolescent populations. N-methyladenosine (mA) is a post-transcriptional modification of RNA, and the most prevalent internal chemical modification of mRNA. KIAA1429, also known as virus-like mA methyltransferase-associated, is a key component of the mA methyltransferase complex, and the largest protein within this complex.

METTL3-mediated SNHG1 mA modification promotes proliferation and migration through transcriptional regulation of WDR74 in osteosarcoma.

Introduction: As the most prevalent internal RNA modification in eukaryotic transcripts, N6-methyladenosine (mA) which is catalyzed by methyltransferase-like 3 (METTL3), is widely involved in cancerous diseases. However, the role of METTL3 and small nucleolar RNA host gene 1 (SNHG1) playing in osteosarcoma (OS) remains largely unknown.

Methods: Bioinformatics analysis, RT-qPCR, western blotting assays were used to detect the expression of METTL3, SNHG1, RNA binding motif protein 15 (RBM15), WD repeat domain 74 (WDR74) and EWS RNA binding protein 1 (EWSR1) accordingly.

SE-lncRNAs in Cancer: Classification, Subcellular Localisation, Function and Corresponding TFs.

Emerging evidence highlights certain long noncoding RNAs (lncRNAs) transcribed from or interacting with super-enhancer (SE) regulatory elements. These lncRNAs, known as SE-lncRNAs, are strongly linked to cancer and regulate cancer progression through multiple interactions with downstream targets. The expression of SE-lncRNAs is controlled by various transcription factors (TFs), and dysregulation of these TFs can contribute to cancer development.

The role of m6A epigenetic modifications in tumor coding and non-coding RNA processing.

Background: Epigenetic modifications of RNA significantly contribute to the regulatory processes in tumors and have, thus, received considerable attention. The m6A modification, known as N6-methyladenosine, is the predominant epigenetic alteration found in both eukaryotic mRNAs and ncRNAs.

Main Body: m6A methylation modifications are dynamically reversible and are catalyzed, removed, and recognized by the complex of m6A methyltransferase (MTases), m6A demethylase, and m6A methyl recognition proteins (MRPs).

METTL3 Mediated MALAT1 m6A Modification Promotes Proliferation and Metastasis in Osteosarcoma Cells.

Background: As one of the most ubiquitous types of posttranscriptional modification, N6-methyladenosine (m6A) is extensively implicated in almost all types of cancers, including osteosarcoma. Our previous research partially uncovered the role of Metastasis Associated Lung Adenocarcinoma Transcript 1 (MALAT1) in osteosarcoma. However, the relationships between methyltransferase-like 3 (METTL3) and noncoding RNAs modified by METTL3, especially MALAT1, in osteosarcoma remain obscure.

N6-methyladenosine (m6A) modification in osteosarcoma: expression, function and interaction with noncoding RNAs - an updated review.

Osteosarcoma, originating from primitive bone-forming mesenchymal cells, is the most common malignant bone tumour among children and adolescents. N6-methyladenosine (m6A), the most ubiquitous type of posttranscriptional modification, is a methylation that occurs in the N6-position of adenosine. m6A dramatically affects the splicing, export, translation, and stability of various RNAs, including mRNA and noncoding RNAs (ncRNAs).

Novel insights into the METTL3-METTL14 complex in musculoskeletal diseases.

N6-methyladenosine (mA) modification, catalyzed by methyltransferase complexes (MTCs), plays many roles in multifaceted biological activities. As the most important subunit of MTCs, the METTL3-METTL14 complex is reported to be the initial factor that catalyzes the methylation of adenosines. Recently, accumulating evidence has indicated that the METTL3-METTL14 complex plays a key role in musculoskeletal diseases in an mA-dependent or -independent manner.

Thoracic ossification of the ligamentum flavum causing Brown-Séquard syndrome: a case report and literature review.

Brown-Séquard syndrome (BSS) has many etiologies, including penetrating trauma, extramedullary tumors, and disc herniation. However, thoracic ossification of the ligamentum flavum (OLF) is an extremely rare cause of this syndrome. A 46-year-old woman with motor weakness in her right lower extremity and urinary retention was admitted to our department.

Circular RNA ROCK1, a novel circRNA, suppresses osteosarcoma proliferation and migration via altering the miR-532-5p/PTEN axis.

As the most prevalent bone tumor in children and adolescents, the pathogenesis and metastasis of osteosarcoma (OS) remain largely unclear. Here, we investigated the expression and function of a novel circular RNA (circRNA), circROCK1-E3/E4, which is back-spliced from exons 3 and 4 of Rho-associated coiled-coil containing protein kinase 1 (ROCK1) in OS. We found that circROCK1-E3/E4, regulated by the well-known RNA-binding protein quaking (QKI), was downregulated in OS and correlated with unfavorable clinical features of patients with OS.

Circular RNAs in osteoporosis: expression, functions and roles.

Osteoporosis, which is caused by an imbalance in osteoblasts and osteoclasts, is a global age-related metabolic disease. Osteoblasts induce osteocyte and bone matrix formation, while osteoclasts play an important role in bone resorption. Maintaining a balance between osteoblast formation and osteoclastic absorption is crucial for bone remodeling.

Accelerating Corrosion of Pure Magnesium Co-implanted with Titanium in Vivo.

Magnesium is a type of reactive metal, and is susceptible to galvanic corrosion. In the present study, the impact of coexistence of Ti on the corrosion behavior of high purity Mg (HP Mg) was investigated both in vitro and in vivo. Increased corrosion rate of HP Mg was demonstrated when Mg and Ti discs were not in contact.

High-purity magnesium interference screws promote fibrocartilaginous entheses regeneration in the anterior cruciate ligament reconstruction rabbit model via accumulation of BMP-2 and VEGF.

Interference screw in the fixation of autologous tendon graft to the bone tunnel is widely accepted for the reconstruction of anterior cruciate ligament (ACL), but the regeneration of fibrocartilaginous entheses could hardly be achieved with the traditional interference screw. In the present work, biodegradable high-purity magnesium (HP Mg) showed good cytocompatibility and promoted the expression of bone morphogenetic protein-2 (BMP-2) and vascular endothelial growth factor (VEGF), fibrocartilage markers (Aggrecan, COL2A1 and SOX-9), and glycosaminoglycan (GAG) production in vitro. The HP Mg screw was applied to fix the semitendinosus autograft to the femoral tunnel in a rabbit model of ACL reconstruction with titanium (Ti) screw as the control.

In vitro and in vivo studies on the degradation of high-purity Mg (99.99wt.%) screw with femoral intracondylar fractured rabbit model.

High-purity magnesium (HP Mg) takes advantage in no alloying toxic elements and slower degradation rate in lack of second phases and micro-galvanic corrosion. In this study, as rolled HP Mg was fabricated into screws and went through in vitro immersion tests, cytotoxicity test and bioactive analysis. The HP Mg screws performed uniform corrosion behavior in vitro, and its extraction promoted cell viability, bone alkaline phosphatase (ALP) activity, and mRNA expression of osteogenic differentiation related gene, i.